Related Experiment Videos
[Effects of beta-blockers and Ca antagonists on diastolic function of the hypertrophied left ventricle: an
Insights
Left ventricular (LV) relaxation is impaired in hypertensive heart disease with LV hypertrophy (HHD) and hypertrophic cardiomyopathy (HCM). Medications like propranolol, pindolol, nifedipine, and diltiazem may improve abnormal LV relaxation in these conditions.
Area of Science:
- Cardiology
- Cardiac Physiology
- Echocardiography
Context:
- Hypertensive heart disease with LV hypertrophy (HHD) and hypertrophic cardiomyopathy (HCM) are conditions characterized by abnormal LV structure.
- Assessing LV relaxation is crucial for understanding diastolic dysfunction in these diseases.
Purpose:
- To investigate left ventricular (LV) relaxation abnormalities in patients with HHD and HCM.
- To evaluate the effects of various medications (propranolol, pindolol, nifedipine, diltiazem) on LV relaxation in these patient groups.
Summary:
- Isovolumic relaxation time (IRT) was significantly prolonged, and peak normalized rate of change of LV cavity in early diastole (peak dD/dt/D) was significantly reduced in HHD patients compared to controls.
- HCM patients showed a trend towards prolonged IRT and reduced peak dD/dt/D.
- A significant inverse relationship was found between peak dD/dt/D and LV wall thickness in HHD.
- Medications, particularly propranolol, pindolol, nifedipine, and diltiazem, demonstrated an improvement in peak dD/dt/D in both HHD and HCM patients, suggesting enhanced LV relaxation.
Impact:
- LV relaxation is demonstrably abnormal in hypertrophied left ventricles, with a strong correlation to increased LV mass in HHD.
- Pharmacological interventions can positively influence LV relaxation in patients with HHD and HCM, offering potential therapeutic strategies.
Abstract:
Left ventricular (LV) relaxation was studied in patients with hypertensive heart disease with LV hypertrophy (HHD, n = 25) and hypertrophic cardiomyopathy (HCM, n = 9), and these data were compared with that of normal controls (n = 20). The effects of oral administration of propranolol (n = 11), pindolol (n = 3), nifedipine (n = 6) and diltiazem (n = 5) in patients with HHD and that of propranolol (n = 9) in patients with HCM were also studied. Isovolumic relaxation time (IRT) was measured using dual M-mode echocardiography and peak normalized rate of change of the LV cavity in early diastole (peak dD/dt/D) was calculated by M-mode echocardiography using a digitizer and microcomputer system. IRT was significantly longer in HHD (112 +/- 24 msec, p less than 0.001) and in HCM (85 +/- 40 msec, p less than 0.05) compared with that of normal subjects (64 +/- 24 msec). The normal value of peak dD/dt/D was 3.8 +/- 0.7 sec-1, and it was significantly lower in HHD (2.7 +/- 0.8 sec-1, p less than 0.001). It was also lower in HCM (3.2 +/- 0.8 sec-1), but without a statistical significance. In HHD there was a significant relationship (r = -0.611, p less than 0.01) between peak dD/dt/D and wall thickness of the LV (interventricular septum + LV posterior wall). There was no significant change in IRT before and after the administration of beta-blockers and calcium antagonists except nifedipine in HHD (before: 116 +/- 28 msec, after: 80 +/- 14 msec, p less than 0.005). It was probably due to the effect of an accompanied decrease in heart rate. However, peak dD/dt/D was significantly increased in both HHD and HCM groups after the administration of propranolol, pindolol, nifedipine and diltiazem. These data show that LV relaxation is abnormal in the hypertrophied LV. Although the genesis of this abnormality is not clear, there seems to be a close relationship between the relaxation abnormality and increased LV mass in HHD. Oral administration of propranolol, pindolol and diltiazem for patients with HHD and propranolol for patients with HCM seems to improve the abnormal LV relaxation of each disease.